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Phosphorylated ERK (pERK) and ERK2 protein expression in esophageal mucosal explants pretreated with either 10 μmol/L of SC-236 (SC 10), 100 μmol/L of SC-236 (SC 100), or dimethyl sulfoxide (DMSO) for 6 hours and treated with either HGF (100 ng/ml) or its vehicle (PBS) for 30 minutes. A: Immunoblotting with anti-phosphorylated Tyr 204 ERK antibody detected the specific 44-kd band for pERK1 protein and the specific 42-kd band for pERK2 protein. Stripping and reprobing with anti-ERK2 antibody showed total ERK2 protein levels. B: Quantitative data for pERK2 levels. Data were obtained by a <t>computerized</t> <t>video</t> <t>analysis</t> of the Western blots. The pERK2 protein levels are expressed as a percentage of total ERK2 protein levels. NS, not significant; *, P < 0.05 versus DMSO + PBS group. Values represent means ± SD. For each column, n = 6.
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Phosphorylated ERK (pERK) and ERK2 protein expression in esophageal mucosal explants pretreated with either 10 μmol/L of SC-236 (SC 10), 100 μmol/L of SC-236 (SC 100), or dimethyl sulfoxide (DMSO) for 6 hours and treated with either HGF (100 ng/ml) or its vehicle (PBS) for 30 minutes. A: Immunoblotting with anti-phosphorylated Tyr 204 ERK antibody detected the specific 44-kd band for pERK1 protein and the specific 42-kd band for pERK2 protein. Stripping and reprobing with anti-ERK2 antibody showed total ERK2 protein levels. B: Quantitative data for pERK2 levels. Data were obtained by a <t>computerized</t> <t>video</t> <t>analysis</t> of the Western blots. The pERK2 protein levels are expressed as a percentage of total ERK2 protein levels. NS, not significant; *, P < 0.05 versus DMSO + PBS group. Values represent means ± SD. For each column, n = 6.
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Phosphorylated ERK (pERK) and ERK2 protein expression in esophageal mucosal explants pretreated with either 10 μmol/L of SC-236 (SC 10), 100 μmol/L of SC-236 (SC 100), or dimethyl sulfoxide (DMSO) for 6 hours and treated with either HGF (100 ng/ml) or its vehicle (PBS) for 30 minutes. A: Immunoblotting with anti-phosphorylated Tyr 204 ERK antibody detected the specific 44-kd band for pERK1 protein and the specific 42-kd band for pERK2 protein. Stripping and reprobing with anti-ERK2 antibody showed total ERK2 protein levels. B: Quantitative data for pERK2 levels. Data were obtained by a <t>computerized</t> <t>video</t> <t>analysis</t> of the Western blots. The pERK2 protein levels are expressed as a percentage of total ERK2 protein levels. NS, not significant; *, P < 0.05 versus DMSO + PBS group. Values represent means ± SD. For each column, n = 6.
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Misoprostol accelerates esophageal ulcer healing and stimulates angiogenesis. Rats were treated intragastrically twice daily with either 50 μg/kg misoprostol or its vehicle for 3 or 6 days starting 3 days after ulcer induction. A: ulcer healing dynamics. Ulcer area was measured by a <t>computerized</t> <t>video</t> <t>analysis</t> of the ulcer images. The results are expressed as a percentage of ulcer area at day 3. Misoprostol treatment significantly reduced ulcer area, reflecting increased esophageal ulcer healing in rats. B: microvessel density in granulation tissue at the ulcer base. The results are expressed as the number of microvessels per square millimeter of granulation tissue section (n/mm2). Misoprostol treatment significantly increased microvessel density (reflecting angiogenesis) in granulation tissue at the esophageal ulcer base. C: proliferating cell nuclear antigen (PCNA) labeling index (LI) in the epithelium at the ulcer margin. The results are expressed as the percentage of increase in the number of labeled cells in the epithelium of the ulcer margin over the number of labeled cells in the epithelium distant from the ulcer. Misoprostol treatment slightly increased epithelial cell proliferation at the esophageal ulcer margin. NS, not significant. Values are means ± SD. For each column (n = 6).
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Misoprostol accelerates esophageal ulcer healing and stimulates angiogenesis. Rats were treated intragastrically twice daily with either 50 μg/kg misoprostol or its vehicle for 3 or 6 days starting 3 days after ulcer induction. A: ulcer healing dynamics. Ulcer area was measured by a <t>computerized</t> <t>video</t> <t>analysis</t> of the ulcer images. The results are expressed as a percentage of ulcer area at day 3. Misoprostol treatment significantly reduced ulcer area, reflecting increased esophageal ulcer healing in rats. B: microvessel density in granulation tissue at the ulcer base. The results are expressed as the number of microvessels per square millimeter of granulation tissue section (n/mm2). Misoprostol treatment significantly increased microvessel density (reflecting angiogenesis) in granulation tissue at the esophageal ulcer base. C: proliferating cell nuclear antigen (PCNA) labeling index (LI) in the epithelium at the ulcer margin. The results are expressed as the percentage of increase in the number of labeled cells in the epithelium of the ulcer margin over the number of labeled cells in the epithelium distant from the ulcer. Misoprostol treatment slightly increased epithelial cell proliferation at the esophageal ulcer margin. NS, not significant. Values are means ± SD. For each column (n = 6).
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Misoprostol accelerates esophageal ulcer healing and stimulates angiogenesis. Rats were treated intragastrically twice daily with either 50 μg/kg misoprostol or its vehicle for 3 or 6 days starting 3 days after ulcer induction. A: ulcer healing dynamics. Ulcer area was measured by a <t>computerized</t> <t>video</t> <t>analysis</t> of the ulcer images. The results are expressed as a percentage of ulcer area at day 3. Misoprostol treatment significantly reduced ulcer area, reflecting increased esophageal ulcer healing in rats. B: microvessel density in granulation tissue at the ulcer base. The results are expressed as the number of microvessels per square millimeter of granulation tissue section (n/mm2). Misoprostol treatment significantly increased microvessel density (reflecting angiogenesis) in granulation tissue at the esophageal ulcer base. C: proliferating cell nuclear antigen (PCNA) labeling index (LI) in the epithelium at the ulcer margin. The results are expressed as the percentage of increase in the number of labeled cells in the epithelium of the ulcer margin over the number of labeled cells in the epithelium distant from the ulcer. Misoprostol treatment slightly increased epithelial cell proliferation at the esophageal ulcer margin. NS, not significant. Values are means ± SD. For each column (n = 6).
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Misoprostol accelerates esophageal ulcer healing and stimulates angiogenesis. Rats were treated intragastrically twice daily with either 50 μg/kg misoprostol or its vehicle for 3 or 6 days starting 3 days after ulcer induction. A: ulcer healing dynamics. Ulcer area was measured by a <t>computerized</t> <t>video</t> <t>analysis</t> of the ulcer images. The results are expressed as a percentage of ulcer area at day 3. Misoprostol treatment significantly reduced ulcer area, reflecting increased esophageal ulcer healing in rats. B: microvessel density in granulation tissue at the ulcer base. The results are expressed as the number of microvessels per square millimeter of granulation tissue section (n/mm2). Misoprostol treatment significantly increased microvessel density (reflecting angiogenesis) in granulation tissue at the esophageal ulcer base. C: proliferating cell nuclear antigen (PCNA) labeling index (LI) in the epithelium at the ulcer margin. The results are expressed as the percentage of increase in the number of labeled cells in the epithelium of the ulcer margin over the number of labeled cells in the epithelium distant from the ulcer. Misoprostol treatment slightly increased epithelial cell proliferation at the esophageal ulcer margin. NS, not significant. Values are means ± SD. For each column (n = 6).
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Misoprostol accelerates esophageal ulcer healing and stimulates angiogenesis. Rats were treated intragastrically twice daily with either 50 μg/kg misoprostol or its vehicle for 3 or 6 days starting 3 days after ulcer induction. A: ulcer healing dynamics. Ulcer area was measured by a <t>computerized</t> <t>video</t> <t>analysis</t> of the ulcer images. The results are expressed as a percentage of ulcer area at day 3. Misoprostol treatment significantly reduced ulcer area, reflecting increased esophageal ulcer healing in rats. B: microvessel density in granulation tissue at the ulcer base. The results are expressed as the number of microvessels per square millimeter of granulation tissue section (n/mm2). Misoprostol treatment significantly increased microvessel density (reflecting angiogenesis) in granulation tissue at the esophageal ulcer base. C: proliferating cell nuclear antigen (PCNA) labeling index (LI) in the epithelium at the ulcer margin. The results are expressed as the percentage of increase in the number of labeled cells in the epithelium of the ulcer margin over the number of labeled cells in the epithelium distant from the ulcer. Misoprostol treatment slightly increased epithelial cell proliferation at the esophageal ulcer margin. NS, not significant. Values are means ± SD. For each column (n = 6).
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Misoprostol accelerates esophageal ulcer healing and stimulates angiogenesis. Rats were treated intragastrically twice daily with either 50 μg/kg misoprostol or its vehicle for 3 or 6 days starting 3 days after ulcer induction. A: ulcer healing dynamics. Ulcer area was measured by a <t>computerized</t> <t>video</t> <t>analysis</t> of the ulcer images. The results are expressed as a percentage of ulcer area at day 3. Misoprostol treatment significantly reduced ulcer area, reflecting increased esophageal ulcer healing in rats. B: microvessel density in granulation tissue at the ulcer base. The results are expressed as the number of microvessels per square millimeter of granulation tissue section (n/mm2). Misoprostol treatment significantly increased microvessel density (reflecting angiogenesis) in granulation tissue at the esophageal ulcer base. C: proliferating cell nuclear antigen (PCNA) labeling index (LI) in the epithelium at the ulcer margin. The results are expressed as the percentage of increase in the number of labeled cells in the epithelium of the ulcer margin over the number of labeled cells in the epithelium distant from the ulcer. Misoprostol treatment slightly increased epithelial cell proliferation at the esophageal ulcer margin. NS, not significant. Values are means ± SD. For each column (n = 6).
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Misoprostol accelerates esophageal ulcer healing and stimulates angiogenesis. Rats were treated intragastrically twice daily with either 50 μg/kg misoprostol or its vehicle for 3 or 6 days starting 3 days after ulcer induction. A: ulcer healing dynamics. Ulcer area was measured by a <t>computerized</t> <t>video</t> <t>analysis</t> of the ulcer images. The results are expressed as a percentage of ulcer area at day 3. Misoprostol treatment significantly reduced ulcer area, reflecting increased esophageal ulcer healing in rats. B: microvessel density in granulation tissue at the ulcer base. The results are expressed as the number of microvessels per square millimeter of granulation tissue section (n/mm2). Misoprostol treatment significantly increased microvessel density (reflecting angiogenesis) in granulation tissue at the esophageal ulcer base. C: proliferating cell nuclear antigen (PCNA) labeling index (LI) in the epithelium at the ulcer margin. The results are expressed as the percentage of increase in the number of labeled cells in the epithelium of the ulcer margin over the number of labeled cells in the epithelium distant from the ulcer. Misoprostol treatment slightly increased epithelial cell proliferation at the esophageal ulcer margin. NS, not significant. Values are means ± SD. For each column (n = 6).
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Misoprostol accelerates esophageal ulcer healing and stimulates angiogenesis. Rats were treated intragastrically twice daily with either 50 μg/kg misoprostol or its vehicle for 3 or 6 days starting 3 days after ulcer induction. A: ulcer healing dynamics. Ulcer area was measured by a <t>computerized</t> <t>video</t> <t>analysis</t> of the ulcer images. The results are expressed as a percentage of ulcer area at day 3. Misoprostol treatment significantly reduced ulcer area, reflecting increased esophageal ulcer healing in rats. B: microvessel density in granulation tissue at the ulcer base. The results are expressed as the number of microvessels per square millimeter of granulation tissue section (n/mm2). Misoprostol treatment significantly increased microvessel density (reflecting angiogenesis) in granulation tissue at the esophageal ulcer base. C: proliferating cell nuclear antigen (PCNA) labeling index (LI) in the epithelium at the ulcer margin. The results are expressed as the percentage of increase in the number of labeled cells in the epithelium of the ulcer margin over the number of labeled cells in the epithelium distant from the ulcer. Misoprostol treatment slightly increased epithelial cell proliferation at the esophageal ulcer margin. NS, not significant. Values are means ± SD. For each column (n = 6).
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Image Search Results


Phosphorylated ERK (pERK) and ERK2 protein expression in esophageal mucosal explants pretreated with either 10 μmol/L of SC-236 (SC 10), 100 μmol/L of SC-236 (SC 100), or dimethyl sulfoxide (DMSO) for 6 hours and treated with either HGF (100 ng/ml) or its vehicle (PBS) for 30 minutes. A: Immunoblotting with anti-phosphorylated Tyr 204 ERK antibody detected the specific 44-kd band for pERK1 protein and the specific 42-kd band for pERK2 protein. Stripping and reprobing with anti-ERK2 antibody showed total ERK2 protein levels. B: Quantitative data for pERK2 levels. Data were obtained by a computerized video analysis of the Western blots. The pERK2 protein levels are expressed as a percentage of total ERK2 protein levels. NS, not significant; *, P < 0.05 versus DMSO + PBS group. Values represent means ± SD. For each column, n = 6.

Journal:

Article Title: Selective Cyclooxygenase-2 Blocker Delays Healing of Esophageal Ulcers in Rats and Inhibits Ulceration-Triggered c-Met/Hepatocyte Growth Factor Receptor Induction and Extracellular Signal-Regulated Kinase 2 Activation

doi:

Figure Lengend Snippet: Phosphorylated ERK (pERK) and ERK2 protein expression in esophageal mucosal explants pretreated with either 10 μmol/L of SC-236 (SC 10), 100 μmol/L of SC-236 (SC 100), or dimethyl sulfoxide (DMSO) for 6 hours and treated with either HGF (100 ng/ml) or its vehicle (PBS) for 30 minutes. A: Immunoblotting with anti-phosphorylated Tyr 204 ERK antibody detected the specific 44-kd band for pERK1 protein and the specific 42-kd band for pERK2 protein. Stripping and reprobing with anti-ERK2 antibody showed total ERK2 protein levels. B: Quantitative data for pERK2 levels. Data were obtained by a computerized video analysis of the Western blots. The pERK2 protein levels are expressed as a percentage of total ERK2 protein levels. NS, not significant; *, P < 0.05 versus DMSO + PBS group. Values represent means ± SD. For each column, n = 6.

Article Snippet: Protein expression was measured using a computerized video analysis system (Image-1/FL, Universal Imaging Corp.).

Techniques: Expressing, Western Blot, Stripping Membranes

COX-1 and COX-2 protein expression in normal esophageal tissue from sham-operated (SO) rats and ulcerated esophageal tissue (UL) 3 and 7 days after sham operation or ulcer induction. A: Immunoblotting with specific antibodies detected the specific 70-kd band for COX-1 and the specific 72-kd band for COX-2. B: Quantitative data for COX-1 and COX-2 protein expression. Data were obtained by a computerized video analysis of the Western blots. NS, not significant; *, P < 0.05 versus UL at 3 days. Values are expressed as optical intensity units and represent means ± SD. For each column, n = 6.

Journal:

Article Title: Selective Cyclooxygenase-2 Blocker Delays Healing of Esophageal Ulcers in Rats and Inhibits Ulceration-Triggered c-Met/Hepatocyte Growth Factor Receptor Induction and Extracellular Signal-Regulated Kinase 2 Activation

doi:

Figure Lengend Snippet: COX-1 and COX-2 protein expression in normal esophageal tissue from sham-operated (SO) rats and ulcerated esophageal tissue (UL) 3 and 7 days after sham operation or ulcer induction. A: Immunoblotting with specific antibodies detected the specific 70-kd band for COX-1 and the specific 72-kd band for COX-2. B: Quantitative data for COX-1 and COX-2 protein expression. Data were obtained by a computerized video analysis of the Western blots. NS, not significant; *, P < 0.05 versus UL at 3 days. Values are expressed as optical intensity units and represent means ± SD. For each column, n = 6.

Article Snippet: Protein expression was measured using a computerized video analysis system (Image-1/FL, Universal Imaging Corp.).

Techniques: Expressing, Western Blot

Effects of celecoxib on esophageal ulcer healing. Ulcer area was measured 3, 5, and 7 days after ulcer induction. Starting from 3 days after ulcer induction, rats were treated with either celecoxib (CEL) (10 mg/kg, once a day) or its vehicle (VHC) for 2 or 4 days. Ulcer area was measured by a computerized video analysis of the ulcers. NS, not significant; *, P < 0.05 versus 3 days. Values are means ± SD. For each column, n = 6.

Journal:

Article Title: Selective Cyclooxygenase-2 Blocker Delays Healing of Esophageal Ulcers in Rats and Inhibits Ulceration-Triggered c-Met/Hepatocyte Growth Factor Receptor Induction and Extracellular Signal-Regulated Kinase 2 Activation

doi:

Figure Lengend Snippet: Effects of celecoxib on esophageal ulcer healing. Ulcer area was measured 3, 5, and 7 days after ulcer induction. Starting from 3 days after ulcer induction, rats were treated with either celecoxib (CEL) (10 mg/kg, once a day) or its vehicle (VHC) for 2 or 4 days. Ulcer area was measured by a computerized video analysis of the ulcers. NS, not significant; *, P < 0.05 versus 3 days. Values are means ± SD. For each column, n = 6.

Article Snippet: Protein expression was measured using a computerized video analysis system (Image-1/FL, Universal Imaging Corp.).

Techniques:

HGF and c-Met protein expression in normal esophageal tissue from sham-operated (SO) rats and ulcerated tissue (UL) 3, 5, and 7 days after sham operation or ulcer induction. Starting from 3 days after ulcer induction, rats were treated with either celecoxib (CEL) (10 mg/kg, once a day) or its vehicle (VHC) for 2 or 4 days. A: Immunoblotting with anti-HGF-α antibody detected the specific 69-kd band for α chain of HGF protein and immunoblotting with anti-c-MET antibody detected a 140-kd band for β-subunit of c-MET protein. B: Quantitative data for HGF protein expression. C: Quantitative data for c-MET protein expression. Data were obtained by a computerized video analysis of the Western blots. NS, not significant; *, P < 0.05 versus UL at 3 days. Values are expressed as optical intensity units and represent means ± SD. For each column, n = 6.

Journal:

Article Title: Selective Cyclooxygenase-2 Blocker Delays Healing of Esophageal Ulcers in Rats and Inhibits Ulceration-Triggered c-Met/Hepatocyte Growth Factor Receptor Induction and Extracellular Signal-Regulated Kinase 2 Activation

doi:

Figure Lengend Snippet: HGF and c-Met protein expression in normal esophageal tissue from sham-operated (SO) rats and ulcerated tissue (UL) 3, 5, and 7 days after sham operation or ulcer induction. Starting from 3 days after ulcer induction, rats were treated with either celecoxib (CEL) (10 mg/kg, once a day) or its vehicle (VHC) for 2 or 4 days. A: Immunoblotting with anti-HGF-α antibody detected the specific 69-kd band for α chain of HGF protein and immunoblotting with anti-c-MET antibody detected a 140-kd band for β-subunit of c-MET protein. B: Quantitative data for HGF protein expression. C: Quantitative data for c-MET protein expression. Data were obtained by a computerized video analysis of the Western blots. NS, not significant; *, P < 0.05 versus UL at 3 days. Values are expressed as optical intensity units and represent means ± SD. For each column, n = 6.

Article Snippet: Protein expression was measured using a computerized video analysis system (Image-1/FL, Universal Imaging Corp.).

Techniques: Expressing, Western Blot

Phosphorylated ERK (pERK), total ERK2 protein expression, and ERK2 activity in normal esophageal tissue from sham-operated (SO) rats and ulcerated tissue (UL) 3, 5, and 7 days after sham operation or ulcer induction. Starting from 3 days after ulcer induction, rats were treated with either celecoxib (CEL) (10 mg/kg, once a day) or its vehicle (VHC) for 2 or 4 days. A: Immunoblotting with anti-phosphorylated Tyr 204 ERK antibody detected the specific 44-kd band for pERK1 protein and the specific 42-kd band for pERK2 protein. Stripping and reprobing with anti-ERK2 antibody showed total ERK2 protein levels. Bottom: Myelin basic protein (MBP) phosphorylated by ERK2 immunoprecipitated from esophageal tissue samples. B: Quantitative data for pERK2 levels. Data were obtained by a computerized video analysis of the Western blots. The pERK2 protein levels are expressed as a percentage of total ERK2 protein levels. C: ERK2 activity determined by measuring levels of radiolabeled [γ-32P]ATP incorporated to MBP by ERK2 (pmol/mg). Values represent means ± SD. For each column, n = 6.

Journal:

Article Title: Selective Cyclooxygenase-2 Blocker Delays Healing of Esophageal Ulcers in Rats and Inhibits Ulceration-Triggered c-Met/Hepatocyte Growth Factor Receptor Induction and Extracellular Signal-Regulated Kinase 2 Activation

doi:

Figure Lengend Snippet: Phosphorylated ERK (pERK), total ERK2 protein expression, and ERK2 activity in normal esophageal tissue from sham-operated (SO) rats and ulcerated tissue (UL) 3, 5, and 7 days after sham operation or ulcer induction. Starting from 3 days after ulcer induction, rats were treated with either celecoxib (CEL) (10 mg/kg, once a day) or its vehicle (VHC) for 2 or 4 days. A: Immunoblotting with anti-phosphorylated Tyr 204 ERK antibody detected the specific 44-kd band for pERK1 protein and the specific 42-kd band for pERK2 protein. Stripping and reprobing with anti-ERK2 antibody showed total ERK2 protein levels. Bottom: Myelin basic protein (MBP) phosphorylated by ERK2 immunoprecipitated from esophageal tissue samples. B: Quantitative data for pERK2 levels. Data were obtained by a computerized video analysis of the Western blots. The pERK2 protein levels are expressed as a percentage of total ERK2 protein levels. C: ERK2 activity determined by measuring levels of radiolabeled [γ-32P]ATP incorporated to MBP by ERK2 (pmol/mg). Values represent means ± SD. For each column, n = 6.

Article Snippet: Protein expression was measured using a computerized video analysis system (Image-1/FL, Universal Imaging Corp.).

Techniques: Expressing, Activity Assay, Western Blot, Stripping Membranes, Immunoprecipitation

Misoprostol accelerates esophageal ulcer healing and stimulates angiogenesis. Rats were treated intragastrically twice daily with either 50 μg/kg misoprostol or its vehicle for 3 or 6 days starting 3 days after ulcer induction. A: ulcer healing dynamics. Ulcer area was measured by a computerized video analysis of the ulcer images. The results are expressed as a percentage of ulcer area at day 3. Misoprostol treatment significantly reduced ulcer area, reflecting increased esophageal ulcer healing in rats. B: microvessel density in granulation tissue at the ulcer base. The results are expressed as the number of microvessels per square millimeter of granulation tissue section (n/mm2). Misoprostol treatment significantly increased microvessel density (reflecting angiogenesis) in granulation tissue at the esophageal ulcer base. C: proliferating cell nuclear antigen (PCNA) labeling index (LI) in the epithelium at the ulcer margin. The results are expressed as the percentage of increase in the number of labeled cells in the epithelium of the ulcer margin over the number of labeled cells in the epithelium distant from the ulcer. Misoprostol treatment slightly increased epithelial cell proliferation at the esophageal ulcer margin. NS, not significant. Values are means ± SD. For each column (n = 6).

Journal: American Journal of Physiology - Gastrointestinal and Liver Physiology

Article Title: Novel mechanisms and signaling pathways of esophageal ulcer healing: the role of prostaglandin EP2 receptors, cAMP, and pCREB

doi: 10.1152/ajpgi.00177.2014

Figure Lengend Snippet: Misoprostol accelerates esophageal ulcer healing and stimulates angiogenesis. Rats were treated intragastrically twice daily with either 50 μg/kg misoprostol or its vehicle for 3 or 6 days starting 3 days after ulcer induction. A: ulcer healing dynamics. Ulcer area was measured by a computerized video analysis of the ulcer images. The results are expressed as a percentage of ulcer area at day 3. Misoprostol treatment significantly reduced ulcer area, reflecting increased esophageal ulcer healing in rats. B: microvessel density in granulation tissue at the ulcer base. The results are expressed as the number of microvessels per square millimeter of granulation tissue section (n/mm2). Misoprostol treatment significantly increased microvessel density (reflecting angiogenesis) in granulation tissue at the esophageal ulcer base. C: proliferating cell nuclear antigen (PCNA) labeling index (LI) in the epithelium at the ulcer margin. The results are expressed as the percentage of increase in the number of labeled cells in the epithelium of the ulcer margin over the number of labeled cells in the epithelium distant from the ulcer. Misoprostol treatment slightly increased epithelial cell proliferation at the esophageal ulcer margin. NS, not significant. Values are means ± SD. For each column (n = 6).

Article Snippet: The ulcer area was measured using a computerized video analysis system (Image 1/FL; Universal Imaging, Westchester, PA).

Techniques: Labeling